Urinary neutrophil gelatinase-associated lipocalin distinguishes pre-renal from intrinsic renal failure and predicts outcomes

Singer, Eugenia; Elger, Antje; Elitok, Saban; Kettritz, Ralph; Nickolas, Thomas L.; Barasch, Jonathan; Luft, Friedrich C.; Schmidt‐Ott, Kai M.

doi:10.1038/ki.2011.41

Cited by 183 publications

(161 citation statements)

References 30 publications

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“…This unexpected finding highlights the contribution of the development of intrinsic AKI during the hospitalization to the overall incidence and importance of potentially modifiable risk factors, such as nephrotoxic medications. Indeed, structural urinary biomarkers such as neutrophil gelatinase-associated lipocalin (NGAL), that are typically upregulated in intrinsic AKI but not in functional prerenal azotemia, are also dramatically elevated in children with NS (21,22). These findings further support the notion that observed AKI is not merely due to intravascular volume depletion.…”

Section: Discussionsupporting

confidence: 74%

AKI in Children Hospitalized with Nephrotic Syndrome

Rheault¹,

Zhang²,

Selewski³

et al. 2015

Clinical Journal of the American Society of Nephrology

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Background and objectives Children with nephrotic syndrome can develop life-threatening complications, including infection and thrombosis. While AKI is associated with adverse outcomes in hospitalized children, little is known about the epidemiology of AKI in children with nephrotic syndrome. The main objectives of this study were to determine the incidence, epidemiology, and hospital outcomes associated with AKI in a modern cohort of children hospitalized with nephrotic syndrome.Design, setting, participants, & measurements Records of children with nephrotic syndrome admitted to 17 pediatric nephrology centers across North America from 2010 to 2012 were reviewed. AKI was classified using the pediatric RIFLE definition.Results AKI occurred in 58.6% of 336 children and 50.9% of 615 hospitalizations (27.3% in stage R, 17.2% in stage I, and 6.3% in stage F). After adjustment for race, sex, age at admission, and clinical diagnosis, infection (odds ratio, 2.24; 95% confidence interval, 1.37 to 3.65; P=0.001), nephrotoxic medication exposure (odds ratio, 1.35; 95% confidence interval, 1.11 to 1.64; P=0.002), days of nephrotoxic medication exposure (odds ratio, 1.10; 95% confidence interval, 1.05 to 1.15; P,0.001), and intensity of medication exposure (odds ratio, 1.34; 95% confidence interval, 1.09 to 1.65; P=0.01) remained significantly associated with AKI in children with nephrotic syndrome. Nephrotoxic medication exposure was common in this population, and each additional nephrotoxic medication received during a hospitalization was associated with 38% higher risk of AKI. AKI was associated with longer hospital stay after adjustment for race, sex, age at admission, clinical diagnosis, and infection (difference, 0.45 [log]days; 95% confidence interval, 0.36 to 0.53 [log]days; P,0.001).Conclusions AKI is common in children hospitalized with nephrotic syndrome and should be deemed the third major complication of nephrotic syndrome in children in addition to infection and venous thromboembolism. Risk factors for AKI include steroid-resistant nephrotic syndrome, infection, and nephrotoxic medication exposure. Children with AKI have longer hospital lengths of stay and increased need for intensive care unit admission.

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Section: Discussionsupporting

confidence: 74%

AKI in Children Hospitalized with Nephrotic Syndrome

Rheault¹,

Zhang²,

Selewski³

et al. 2015

Clinical Journal of the American Society of Nephrology

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“…These biomarkers displayed a progressive increase across the spectrum of AKI (no AKI , prerenal , intrinsic). Although the definition of prerenal AKI used is not universally accepted, this investigation of a mixed medical-surgical ICU population corroborates a previous single-center study that showed that biomarkers may help distinguish between prerenal and intrarenal causes of AKI (43). Our hope is that, in the near future, investigations move away from nonstandardized and potentially confusing terms such as prerenal and view kidney injury in terms of biomarkers of functional and structural damage.…”

Section: Biomarkers In the Setting Of Critical Illness And Sepsissupporting

confidence: 61%

“…After adjusting for clinical covariates known to impact critical illness and AKI, UCysC levels were independently associated with sepsis (OR=3. 43 (32). Note, in this study, that there was no interaction between sepsis and AKI and that these findings are in line with smaller studies that investigated the ability of UCysC to detect early AKI and predict the need for RRT and death in a mixed surgical and medical ICU population (34,35).…”

Section: Biomarkers In the Setting Of Critical Illness And Sepsismentioning

confidence: 99%

Clinical Utility of Biomarkers of AKI in Cardiac Surgery and Critical Illness

Koyner

Parikh

2013

Clinical Journal of the American Society of Nephrology

100

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SummaryAKI is a common and serious complication that is associated with several adverse outcomes in hospitalized patients. The past several years have seen a large number of multicenter investigations of biomarkers of AKI in the setting of cardiac surgery and critical illness. This review summarizes these biomarker results to identify applications for clinical use. The Translational Research Investigating Biomarker Endpoints in AKI (TRIBE-AKI) study showed that blood and urine biomarkers measured preoperatively, immediately postoperatively, and at the time of the clinical increase in serum creatinine in the setting of cardiac surgery all had the ability to improve patient risk stratification for a variety of important clinical end points. Analyses of biomarkers concentrations from the Acute Respiratory Distress Syndrome Network, EARLY ARF, and other studies of critically ill subjects have similarly shown that biomarkers measured early in the clinical course can forecast the development of AKI and need for renal replacement therapy as well as inpatient mortality. Although biomarkers have informed the diagnosis, prognosis, and treatment of AKI and are inching closer to clinical application, large multicenter interventional clinical trials to prevent AKI using biomarkers should continue to be an active area of clinical investigation.

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“…63 GVHD may therefore contribute to kidney injury fundamentally by two mechanisms: directly through cytokine-and immune-related injury, including glomerular deposits triggering nephrotic syndrome, and tubulitis; or indirectly through nephrotoxicity induced by calcineurin inhibitors used as prophylaxis against GVHD. 17,18 Moreover, GVHD-associated nephrotoxicity may result from severe GVHD with diarrhea and subsequent dehydration, as well as from CMV reactivation because of GVHD treatment with high-dose prednisolone. 7,19 An augmented risk of the development of AKI in non-myeloablative HCT has been linked to CMV reactivation in itself.…”

Section: Pathogenesismentioning

confidence: 99%

Acute kidney injury in HCT: an update

Lopes

Jorge

Neves

2016

Bone Marrow Transplant

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Acute kidney injury (AKI) is highly prevalent whether the patients undergo myeloablative or non-myeloablative hematopoietic cell transplantation (HCT); however, the pathogenesis and risk factors leading to AKI can differ between the two. The prognosis of AKI in patients receiving HCT is poor. In fact, AKI following HCT is associated not only with increased short-and long-term mortality, but also with progression to chronic kidney disease. Herein, the authors provide a comprehensive and up-to-date review of the definition and diagnosis, as well as of the incidence, pathogenesis and outcome of AKI in patients undergoing HCT, centering on the differences between myeloablative and non-myeloablative regimens. INTRODUCTIONHematopoietic cell transplantation (HCT) is currently used to treat numerous malignant (for example, multiple myeloma, leukemias and lymphomas) and non-malignant hematological disorders (for example, aplastic anemia, b-thalassemia, immunodeficiency disorders and inborn errors of metabolism), as well as solid tumors (for example, breast cancer and neuroblastoma), which are in other instances incurable.The two major HCT procedures, taking into consideration the conditioning regimen used, are myeloablative autologous and allogeneic HCT and non-myeloablative allogeneic HCT. On the one hand, myeloablative HCT utilizes the maximally tolerated dose of TBI with or without chemotherapy, or with chemotherapy alone. On the other hand, non-myeloablative HCT depends more on donor cellular immune effects and less on the cytotoxic effects of the preparative regimen to control the underlying disease. 1,2 It ultimately uses a lower dose conditioning regimen and can thus be offered to older patients, to those debilitated by additional comorbidities, or to high-risk, heavily pretreated patients, who would not tolerate myeloablative HCT, resulting in a consequent decrease in regimen-related toxicity and treatment-related mortality. [3][4][5] Acute kidney injury (AKI) is highly prevalent whether the patients undergo myeloablative or non-myeloablative regimens; however, the pathogenesis and risk factors leading to AKI can differ between the two. In fact, AKI in patients receiving HCT is associated not only with increased short-and long-term mortality as compared with patients with no AKI, but also with a higher rate of progression to chronic kidney disease (CKD). Herein, the authors provide a comprehensive and up-to-date review of the definition and diagnosis of AKI as well as of the incidence, risk factors, pathogenesis and outcome of AKI in patients undergoing HCT, centering on the differences between myeloablative and nonmyeloablative regimens.

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Urinary neutrophil gelatinase-associated lipocalin distinguishes pre-renal from intrinsic renal failure and predicts outcomes

Cited by 183 publications

References 30 publications

AKI in Children Hospitalized with Nephrotic Syndrome

AKI in Children Hospitalized with Nephrotic Syndrome

Clinical Utility of Biomarkers of AKI in Cardiac Surgery and Critical Illness

Acute kidney injury in HCT: an update

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